Chronic Alcoholism in man is associated with swelling and fragmentation of mitochondrial and microsomal membranes in heart tissue. We have documented changes in the total fatty acid patterns in hearts of chronically treated rats. The main changes were an increase in the linoleate content and a decrease in the arachidonate content. We have also demonstrated that chronic alcohol ingestion leads to a decrease in the oxidation of fatty acids by the heart; however, this decrease in Beta-oxidation does not explain the decrease in the arachidonate concentration. Since fatty acids are major components of membranes and since alcohol ingestion interferes with the metabolism of fatty acids and produces abnormalities in the membranes, we propose to continue our studies of lipid metabolism in the heart and the effects of chronic alcohol ingestion thereon. We will continue our studies on the Beta- oxidation of individual fatty acids with special emphasis on arachidonate. We have studied palmitate, stearate, oleate and linoleate so far. We will also try to determine if alcohol enhances lipid peroxidation in the heart as we have demonstrated in the liver. Since arachidonate is more highly unsaturated than linoleate, these studies might provide an answer to the fatty acid content changes. Also in the same area, we will measure the effects of alcohol on the chain elongation - desaturation system which synthesizes arachidonate from linoleate. Other studies which we propose concern the effects of alcohol on the acyl-CoA:phospholipid acyltransferases which are responsible for the restructuring of the phospholipids which in turn are vital components of the membranes. Changes noted in acyltransfer rates might aid in assertaining the mechanism leading to the membrane changes. From the results of these studies it is hoped that we can explain the fatty acid changes noted and then possibly pose a hypothesis for the membrane abnormalities in chronic alcoholic heart disease.